Abstract
Mitochondria are dynamic organelles, the morphology of which is tightly linked to their functions. The interplay between the coordinated events of fusion and fission that are collectively described as mitochondrial dynamics regulates mitochondrial morphology and adjusts mitochondrial function. Over the last few years, accruing evidence established a connection between dysregulated mitochondrial dynamics and disease development and progression. Defects in key components of the machinery mediating mitochondrial fusion and fission have been linked to a wide range of pathological conditions, such as insulin resistance and obesity, neurodegenerative diseases and cancer. Here, we provide an update on the molecular mechanisms promoting mitochondrial fusion and fission in mammals and discuss the emerging association of disturbed mitochondrial dynamics with human disease.
Highlights
Dysregulation of MitochondrialMitochondria represent a tubular, remarkably dynamic system of membrane-bound cell organelles that were first observed in high-resolution electron micrographs in the early1950s [1]
The delicate equilibrium between fusion and fission confers important benefits that are brought about through the exchange of mitochondrial content, maintenance of their genome and segregation of dysfunctional organelles that are targeted for autophagic degradation [10], a mitochondrial quality-control process known as mitophagy
Both MFN1 and MFN2 are targeted to the outer mitochondrial membrane (OMM), MFN2 is localized on endoplasmic reticulum (ER) membranes, where it mediates the physical association between the ER and mitochondria [30]
Summary
Mitochondria represent a tubular, remarkably dynamic system of membrane-bound cell organelles that were first observed in high-resolution electron micrographs in the early. The delicate equilibrium between fusion and fission confers important benefits that are brought about through the exchange of mitochondrial content, maintenance of their genome and segregation of dysfunctional organelles that are targeted for autophagic degradation [10], a mitochondrial quality-control process known as mitophagy. This selective form of autophagy acts in concert with mitochondrial biogenesis for the control of mitochondrial turnover. Perturbations in the dynamic transitions of the mitochondrial network caused by aberrant fusion and fission will be highlighted in the context of representative human diseases
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